ライフサイエンスコーパス: sodium retention

1 pulmonary hypertension, muscle weakness, and sodium retention.

2 igh plasma aldosterone and increased urinary sodium retention.

3 rough aldosterone binding and stimulation of sodium retention.

4 vity, sympathetic nervous activity and renal sodium retention.

5 y depressed plasma renin activity because of sodium retention.

6 nin-angiotensin-aldosterone system (RAAS) or sodium retention.

7 ase blood pressure, catecholamine levels, or sodium retention.

8 e rats several renal abnormalities encourage sodium retention.

9 de (ANP) characterize states of pathological sodium retention.

10 ectly on the renal tubule is responsible for sodium retention.

11 uces albuminuria without causing significant sodium retention.

12 lance fluid homeostasis during conditions of sodium retention.

13 the NLRP3 inflammasome, with consequences on sodium retention.

14 via NCC activation at the cost of increasing sodium retention.

15 sine is not responsible for vasodilation and sodium retention, (2) a sodium-retaining factor acting d

16 n of proinflammatory adipokines that lead to sodium retention and cardiac steatosis and fibrosis.

17 In contrast, severe CHF is characterized by sodium retention and coactivation of both ANP and the RA

18 aldosterone, which synergistically stimulate sodium retention and consumption.

19 o be selective for inhibition of COX-2 cause sodium retention and elevate blood pressure.

20 hypertension have not been established, but sodium retention and excessive sympathetic tone are key

21 Sodium retention and gamma-ENaC cleavage were independen

22 sodium transporters that are obligatory for sodium retention and hypertension in response to nitric

23 ney distal tubule (DT), leading to increased sodium retention and hypertension.

24 anesthesia in portal hypertensive rats with sodium retention and in sham-operated controls.

25 dysfunction and damage, leading to enhanced sodium retention and increased systemic vascular resista

26 The mechanism of sodium retention and its location in kidney tubules may

27 This appears to be independent of renal sodium retention and may contribute to hypertension in 1

28 Normal pregnancy is also accompanied by sodium retention and plasma volume expansion, and pregna

29 es renal renin production and produces renal sodium retention and renin-dependent hypertension.

30 However, whether T cells contribute to renal sodium retention and salt-sensitive hypertension is unkn

31 pressure-natriuresis relation in the kidney, sodium retention, and compensatory nocturnal natriuresis

32 inished renal potassium excretion, excessive sodium retention, and hypertension (pseudohypoaldosteron

33 role in CNI-induced renal vasoconstriction, sodium retention, and hypertension.

34 itor MCC950 reversed the hypertensive state, sodium retention, and renal transporter activation.

35 pertension is most often caused by excessive sodium retention, and that spironolactone would therefor

36 creasing the circulatory flow, thus reducing sodium retention, ascites recurrence, and variceal bleed

37 ed by a suppressed plasma renin level due to sodium retention but manifests in eNOS uncoupling; howev

38 itors, muscle weakness by exercise training, sodium retention by diuretics and monitoring devices, my

39 These sex differences potentiate sodium retention by males and increase kidney function d

40 al COX-2 activity and subsequent increase in sodium retention by the kidney.

41 tance, increases in plasma volume induced by sodium retention can manifest as a rise in systemic arte

42 This pathway may play a role in sodium retention caused by activation of PPARgamma in ma

43 n day 1 after surgery when transient maximal sodium retention developed and day 7 when rats returned

44 brain Galphai(2) proteins, animals exhibited sodium retention, global sympathoexcitation, and elevate

45 ccupies mineralocorticoid receptors, causing sodium retention, hypokalemia, and hypertension.

46 by diuretics, diuretic resistance, and renal sodium retention in edematous states.

47 on of cGMP in response to ANP contributes to sodium retention in heart failure, but may be compensate

48 s a major determinant of the tubular site of sodium retention in nephrotic mice.

49 insic sodium transport abnormality linked to sodium retention in nephrotic syndrome.

50 Hypertension is attributed to sodium retention in the distal nephron, but 11betaHSD2 i

51 tenderness and bloating did not result from sodium retention in the luteal phase of the menstrual cy

52 The mechanism responsible for the renal sodium retention in these mice is largely unknown.

53 of spironolactone supports a primary role of sodium retention in this condition.

54 We studied the mechanisms of sodium retention in transgenic POD-ATTAC mice, which dis

55 Distal tubular sodium retention is a potent driver of hypertension, and

56 As COX inhibition is often associated with sodium retention leading to edema and hypertension, pros

57 ogical mechanisms in HFpEF and DM, including sodium retention, metabolic derangements, impaired skele

58 ce compared with controls suggest that early sodium retention occurs mainly in the proximal and dista

59 This may contribute to the physiologic sodium retention of normal pregnancy.

60 eased renal PDE5 activity in the physiologic sodium retention of normal rat pregnancy.

61 The hematopoietic Tet2(-/-) condition led to sodium retention, renal inflammasome activation, and ele

62 ontribute to hypertension by promoting renal sodium retention, renin release and renal vasoconstricti

63 Sodium retention required diuretic therapy, and mild hyp

64 natriuretic peptide (ANP) and the excessive sodium retention seen in experimental nephrotic syndrome

65 These findings indicate that sodium retention shifted from the proximal and distal tu

66 ack patients also shows clinical features of sodium retention so we screened black people for the T59

67 adenosine in the peripheral vasodilation and sodium retention that occurs after partial portal vein l

68 ne conditions, portal hypertensive rats with sodium retention were hypotensive, with decreases in tot

69 unction of D1 receptors results in increased sodium retention which can potentially lead to the devel

70 tes results from sinusoidal hypertension and sodium retention, which is in turn secondary to vasodila

71 tes results from sinusoidal hypertension and sodium retention, which is, in turn, secondary to vasodi

72 tes results from sinusoidal hypertension and sodium retention, which, in turn, is secondary to vasodi